NEONATAL

SEIZURES

Postgraduate
Dept of pediatrics
 OBJECTIVES
To familiarize the varied presentations of
neonatal seizures.
To distinguish non seizure states from seizures.

To recognize the unique etiology of neonatal

seizures.
To familiarize the algorithm of management
specific to neonatal seizures.
To be able to decide the duration of antiepileptic
therapy and followup.
OVERVIEW

DEFINITION OF SEIZURE
TYPES OF NEONATAL SEIZURES

CAUSES OF NEONATAL SEIZURES

SEIZURE MIMICS

APPROACH TO NEONATAL SEIZURES

DURATION OF ANTICONVULSANT THERAPY

GUIDELINES
PROGNOSIS
 SEIZURE is defined clinically as paroxysmal
alteration in neurologic function ie., motor, behaviour
and/or autonomic function.
It includes
1. Epileptic seizures - phenomenon associated with
corresponding EEG seizure activity.
Eg: clonic seizures.
2. Nonepileptic seizures - clinical seizures without
corresponding EEG correlate.
Eg: subtle and generalised tonic seizures.
3. EEG seizures - abnormal EEG activity with no
clinical correlation.
EPIDEMIOLOGY- INDIA(NNPD;2002-03)
Incidence : 10.3 per 1000 live births
The incidence is high in PRETERM
neonates (2 fold), VLBW( 4 fold) compared
to TERM neonates.
Term neonates- 8.4
Preterm neonates-20.8
VLBW-36.1
Why seizures are common in neonatal
period ?

Seizures are common in neonatal period than any

other time in life due to decreased seizure threshold.

Transient overdevelopment of excitatory system than

inhibitory system.
Why generalised seizures are rare in
neonates ?

Neonatal brain has reduced connectivity,

therefore electrical discharges spread
incompletely, so generalised seizures are rare
in neonates.
TYPES OF NEONATAL SEIZURES

Four major types of neonatal seizures

1. Subtle seizures
2. Clonic seizures
3. Tonic seizures
4. Myoclonic seizures
 SUBTLE SEIZURES
Most common form(>50%)
It includes

a) Ocular - tonic horizontal deviation of eyes or sustained

eye opening with ocular fixation or cycled fluttering.
b) Oral facial lingual movements - chewing, tongue
thrusting, lip smacking etc.
c) Limb movements - cycling, paddling, boxing etc.
d) Autonomic phenomena-tachycardia or bradycardia.
e) Apnea may be a rare manifestation of seizure.
CLONIC SEIZURES

Rhythmic movements of muscle groups.

Have both fast and slow movements with frequency of
1-3 jerks per second.
Commonly associated with EEG changes.

May be unifocal or multifocal.

Focal clonic has good prognosis.

TONIC SEIZURES
Pattern is sustained posture of limbs or
asymmetrical truncal postures.

cause: diffuse neurological injury or IVH in

preterm or postasphyxial.
Usually no EEG changes.

Prognosis is poor except for postasphyxial cases.

 MYOCLONIC SEIZURES
Non rhythmic lightning fast contraction.

Seen in diffuse brain damage as in perinatal

asphyxia, inborn errors of metabolism, cerebral
dysgenesis.

Worst prognosis in terms of neurodevelopmental

outcome and seizure recurrence.
CAUSES OF NEONATAL SEIZURES
AGES 1 - 4 DAYS

HIE
( most common )

IVH

Acute
metabolic disorder
hypocalcemia
hypoglycemia
hypomagnesemia
hypo/ hypernatremia
 Drugwithdrawl maternal drug use of
narcotics or barbiturates.

Drug toxicity- lidocaine, penicillin.

Inbornerrors of metabolism galactosemia,

hyperglycinemia, urea cycle disorders.

Pyridoxine deficiency (must be considered at all

ages).
 AGES 4 - 14 DAYS

Infection meningitis (bacterial) , encephalitis

(enteroviral, herpes simplex).
Metabolic disorders hypocalcemia, hypoglycemia

Drug withdrawal

Kernicterus, hyperbilirubinemia

Benign neonatal convulsions

Developmental delay, epilepsy, neonatal diabetes

syndrome- DEND syndrome
 AGES 2 - 8 WEEKS

Infection
Head injury subdural hematoma

Inherited disorders of metabolism - aminoacidurias ,

organic aciduria, urea cycle defects
Malformations of cortical developments

lissencephaly, focal cortical dysgenesis.

Tuberous sclerosis

Sturge weber syndrome

SPECIFIC ETIOLOGIES
Hypoxic Ischemic Encephalopathy

Most common cause of neonatal seizures usually

in the first 24 hours.

In perinatal asphyxia, seizures occur in context of

history of difficulty during labour , delivery with
fetal HR alterations, low Apgar scores.
Intra cranial hemorrhages

Sub arachnoid hemorrhages cause seizures

usually on second day and have a very good
outcome.
In preterm infant, seizures occur with
extension of germinal matrix hemorrhage to
parenchyma typically after 3 days of life and it
is not assosciated with good outcome.
 Acute metabolic disorders

Hypoglycemia

Hypocalcemia : Whole blood ionized calcium is the

best measure.
ionised calcium < 1.1 mmol/lit in > 1500gm.
ionised calcium < 1 mmol/lit in < 1500gm.
Hypomagnesemia: Levels < 1.4mg/dl (0.6 mmol/lit )
are considered low.
Hypo/Hypernatremia
 Neonatal seizure syndromes

Benign familial neonatal seizures

Benign idiopathic neonatal seizures ( fifth day fits )

Early infantile epileptic encephalopathy ( Ohtahara

syndrome )
Malignant migrating partial seizures ( Coppala
syndrome )
 SEIZURE MIMICS
1. Jitteriness suppress with passive flexion,
increases with stimulation, not associated with
autonomic accompaniments and eye movements.
2.Epileptic apnea associated with tachycardia.
3.Benign neonatal sleep myoclonus - occur as
synchronus myoclonic jerks during REM sleep
disappear when baby is awake, EEG is normal
and spontaneously resolve by 2 months of age.
Clinical seizures jitteriness
character
Increases with rare common
stimulation
Suppress with absent present
passive flexion
Autonomic present absent
phenomena
Eye or facial present absent
movements
Rate of Clonic seizures show Rate of movement
movement rapid alteration of fast is identical in
and slow phase of either direction.
APPROACH TO NEONATAL
SEIZURES
 HISTORY

Seizure history regarding type of seizure ,

associated movements , day of onset.

Antenatal history - intrauterine infection , maternal

diabetes , narcotic addiction.

Perinatal history - H/o fetal distress, instrumental

delivery, need for resuscitation in labour room, apgar
scores .
 Feeding history appearance of lethargy, poor
activity and vomiting after initiation of breast feeding
may be suggestive of IEM.

Family history H/o consanguinity in parents ,

family h/o seizures or MR , early fetal or neonatal
deaths would be suggestive of IEM.
H/o seizures in either parent or sibling in neonatal
period may be suggestive of benign familial neonatal
convulsion.
 EXAMINATION

Vitals HR, RR, CRT, Temp, BP.

General examination gestation , birth wt and wt

for age
- Seizures in term well baby may be due to SAH.
- Seizures in large for date babies may be due to
hypoglycemia.
 CNS examination presence of bulging AF may be
suggestive of meningitis or ICH
- consciousness (alert /drowsy/comatose).
- tone (hypo/hyper).
- fundus examination for chorioretinitis.

Systemic examination presence of

hepatosplenomegaly or abnormal urine odour may
be suggestive of IEM
- skin should be examined for neurocutaneous
markers .
INVESTIGATIONS
Essential
- Blood sugar
- Serum electrolytes
- CSF examination
- Cranial ultrasound
- EEG
 Additional
Hematocrit (if plethoric and/or at risk for
polycythemia)
Serum bilirubin (if icteric)
Serum magnesium
Arterial blood gas and anion gap (lethargy,
vomiting, family history, etc.)
Imaging: CT and/or MRI (if no etiology found
after essential investigations)
TORCH screen for congenital infections
Work-up for inborn errors of metabolism
 NSG - excellent tool for detection of IVH and
parenchymal hemorrhage.

CT - diagnostic in SAH and developmental

malformations.

MRI - diagnostic in cerebral dysgenesis, lissencephaly

and other neuronal migration disorders.

EEG - diagnostic and prognostic role in seizures and

should be done in all neonates who need
anticonvulsant treatment.
Acute management of
seizures
 Neonate with seizures

Identify and characterize the seizure

Secure airway and optimize breathing, circulation, and temperature
Secure IV access and take samples for baseline investigations

If hypoglycemic : administer 2 ml/kg of 10% dextrose as

bolus followed by a continuous infusion of 6-8 mg/kg/min

If serum calcium is abnormal, 2 ml/kg of calcium gluconate

(10%) should be given IV under cardiac monitoring

Seizures persist
 Administer phenobarbitone 20mg/kg IV stat
over 20 minutes
Seizures
continue
Repeat phenobarbitone in 10 mg/kg/dose
aliquots until 40 mg/kg dose is reached
Seizures continue

Administer phenytoin 20 mg/kg IV slowly

over 20 minutes under cardiac monitoring
Seizures continue

Lorazepam: 0.05 mg/kg IV bolus over 2-5 minutes; may be repeated

Midazolam: 0.15 mg/kg IV bolus followed by infusion of 1-7 mcg/kg/min
Clonazepam 0.1mg/kg;Consider ventilation.
Seizures continue
 Second line drugs like
Lidocaine[4mg/kg f/b 2mg/kg/hr]
Paraldehyde[0.1-0.2ml/kg/dose IM]
sodium valproate[20-25mg/kg f/b 5-10mg/kg/12h]
Topiramate(20mg/kg/day)
Levetiracetam(10-30mg/kg/day)
Vigabatrin(50mg/kg/day) Pyridoxine(100mgIVtestdose)
exchange transfusion[IEMs,drug toxicity,bilirubin encephalopathy ]

Seizures controlled

Wean AEDs slowly to maintenance

phenobarbitone
 MAINTENANCE DOSE
Phenobarbitone or phenytoin after
loading dose maintenance dose 3-5
mg/kg/day in two divided doses.
Wean slowly in a way, taper the last
given anti convulsant first and first
given phenobarbitone in last.
DURATION OF
ANTICONVULSANT
THERAPY GUIDELINES
 Newborn on anticonvulsant therapy

Wean all antiepileptic drugs except phenobarbitone once seizure

controlled

Perform neurological examination prior to discharge

Normal Abnormal

Stop Continue phenobarbitone for 1 month

phenobarbitone
prior to
Repeat neurological examination at 1 month
discharge

Normal examination Abnormal examination

Evaluate EEG
Taper drugs Abnormal EEG
Normal EEG Continue drug;
over 2 weeks Taper drugs over reassess at 3
2 weeks
 PROGNOSIS
Focal clonic seizures carry the best prognosis.
Myoclonic seizures carry the worst prognosis in

terms of neurodevelopmental outcome and

seizure recurrence.
Seizures due to SAH and late onset hypocalcemia
carry best prognosis in terms of long term
neurodevelopmental outcome.
Seizures related to hypoglycemia,cerebral
malformations and meningitis have adverse
outcome.
 Neurological Disease Normal
Development

Hypoxic-ischemic encephalopathy 50%

Primary subarachnoid hemorrhage 90%

Hypocalcemia
Early-onset 50%
Later-onset 100%

Hypoglycemia 50%
Bacterial meningitis 50%
 SUMMARY
Seizures are common in neonatal period than any
other period of life.
Subtle seizures are the most common type of
neonatal seizures.
Hypoxic ischemic encephalopathy is the most
common cause of neonatal seizures.
Phenobarbitone is the drug of choice for neonatal
seizures.
Focal clonic seizures and seizures due to
subarachnoid hemorrhage and late onset
hypocalcemia carries best prognosis.
 REFERENCES
AIIMS NICU PROTOCOL
PGEI NICU PROTOCOL

MANUAL OF NEONATAL CARE - CLOHERTY

NELSON TEXTBOOK OF PEDIATRICS

CARE OF THE NEWBORN MEHARBAN

SINGH
PRACTICAL PEDIATRIC NEUROLOGY
VEENA KALRA
IAP TEXT BOOK OF PEDIATRICS
THANK YOU